POS0270 DEVELOPMENT OF AORTIC ANEURYSM/DILATATION IN A PROSPECTIVE COHORT OF PATIENTS WITH BIOPSY-PROVEN GIANT-CELL ARTERITIS: EARLY IDENTIFICATION OF PATIENTS AT RISK.
Authors: J. Marco Hernandez, A. García-Martínez, S. Prieto-González, A. Suso, G. Espígol-Frigolé, P. Arguis, R. Gilabert, M. Alba, J. Hernández-Rodríguez, M. C. Cid
Journal: Annals of the Rheumatic Diseases (2022)

Background Up to 10-33% of patients with giant-cell arteritis (GCA) develop aortic structural damage (ASD) (aneurysm or dilatation), typically involving the ascending aorta (1,2). Systematic use of imaging reveals radiological features of aortitis in 45-65% of patients at diagnosis (3). This finding has been associated with future aortic dilatation in retrospective studies (4). Objectives To investigate the prevalence of thoracic ASD in a large prospective cohort of patients with GCA subjected to periodic imaging. To evaluate the association between features at diagnosis with ASD development. Methods Patients were included in the study if consented, had biopsy-proven GCA and met the 1990 ACR criteria for GCA classification. Patients were prospectively followed and treated according to uniform criteria. Since 1995 patients were subjected to systematic imaging screening aimed to detect thoracic ASD. Until November 2006 it consisted of a chest X-ray that was performed at least 4 years after diagnosis and repeated every 4 years. When aortic dilatation was minimally suspected, patients underwent contrast-enhanced computed tomography (CT) scan. Since November 2006, most of patients were prospectively studied with CT angiography at diagnosis, after 1 year and every 4 years. The diagnosis of ASD was confirmed by CT, defined as an aortic diameter &gt; 4 cm at the ascending aorta or ≥4 cm at the aortic arch or the descending aorta. Data regarding demographic characteristics, cardiovascular risk factors, GCA symptoms, laboratory tests, chronic medication at time of GCA diagnosis and corticosteroid tapering were recorded. Kaplan-Meier survival plot was used to present the cumulated incidence of thoracic ASD over time and patients were censored at the time of ASD diagnosis or at the time of the last screening in those without ASD. We also investigated which variables present at the time of GCA-diagnosis were associated with future development of ASD. Patients were classified in two groups according to whether they developed ASD or not during a follow-up period of 8 ± 1 years from the time of diagnosis. Results Thoracic ASD was confirmed by CT in 58 patients (21.6% of the patients with systematic screening diagnosed from 1994 to 2018) after a median follow-up of 4.7 years (0.05-7.5). Ascending aorta was involved in 56 patients (96.5%), followed by the aortic arch in 11 patients (18.9%), and descending aorta in 5 (8.6%). 14 patients (24.1%) had more than 1 aortic segment involved. Figure 1 shows the number of patients with thoracic ASD detected during follow-up. Figure 1. Thoracic ASD was detected within the first 4 years from GCA-diagnosis in 19 out of the 58 patients who developed ASD (32.7%) but was severe (≥ 50 mm) in only 3 (15.8% out of those 19 patients). Most ASD was detected between 5 and 9 years after GCA-diagnosis. Patients who developed ASD during follow-up experienced less often cranial ischemic symptoms (14.8% vs 41.1%; p=0.003) or polymyalgia (33.3% vs 51.8%; p=0.057), and less frequently had a previous diagnosis of hypertension (66.7% vs 82.1%; p=0.081). Age, sex, clinical or laboratory findings or chronic therapies used at time of GCA-diagnosis were not significantly different between groups. After multivariate analysis, the presence of cranial ischemic symptoms (HR 0.180, 95% CI 0.065-0.495, p=0.001) and polymyalgia rheumatica (HR 0.329, 95% CI 0.136-0.793, p=0.013) remained inversely associated with thoracic ASD development. Conclusion ASD is frequent and probably an underdiagnosed complication of GCA. There is no consensus yet regarding the optimal screening protocol during follow-up and early identification of patients at risk is crucial for this purpose. The presence of cranial ischemic symptoms or polymyalgia rheumatica were inversely associated with thoracic ASD development in our prospective cohort. References [1]García-Martínez A et al. Ann Rheum Dis 2014. [2]Evans JM et al. Ann Intern Med 1995. [3]Prieto-González S et al. Ann Rheum Dis 2012. [4]Blockmans D et al. Rheumatology (Oxford) 2008. Acknowledgements Both first co-authors contributted equally to this work. The research was supported MTV3 2014/20150730 Disclosure of Interests None declared